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ORIGINAL ARTICLE
Year : 2014  |  Volume : 10  |  Issue : 37  |  Page : 92-99

Silybum marianum oil attenuates oxidative stress and ameliorates mitochondrial dysfunction in mice treated with D-galactose


1 Department of Food Quality and Safety, School of Food and Biological Engineering, Jiangsu University, Zhenjiang, Jiangsu, 212013, China
2 Department of Food Science and Engineering, School of Food and Biological Engineering, Jiangsu University, Zhenjiang, Jiangsu, 212013, China

Correspondence Address:
Ying Dong
Department of Food Science and Engineering, School of Food and Biological Engineering, Jiangsu University, 301 Xuefu Road, Zhenjiang, Jiangsu Province, 212013
China
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Source of Support: This work was supported by Grants from the Agricultural Science and Technology Support Program of Zhenjiang (NY2012031) and Innovation project for postgraduate education of Jiangsu province (CX 07B_182z), Conflict of Interest: None


DOI: 10.4103/0973-1296.127353

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Background: Silybum marianum has been used as herbal medicine for the treatment of liver disease, liver cirrhosis, and to prevent liver cancer in Europe and Asia since ancient times. Silybum marianum oil (SMO), a by-product of silymarin production, is rich in essential fatty acids, phospholipids, sterols, and vitamin E. However, it has not been very good development and use. Objective: In the present study, we used olive oil as a control to investigate the antioxidant and anti-aging effect of SMO in D-galactose (D-gal)-induced aging mice. Materials and Methods: D-gal was injected intraperitoneally (500 mg/kg body weight daily) for 7 weeks while SMO was simultaneously administered orally. The triglycerides (TRIG) and cholesterol (CHOL) levels were estimated in the serum. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), monoamine oxidase (MAO), malondialdehyde (MDA), caspase-3, and Bcl-2 were determined in the liver and brain. The activities of Na + -K + -adenosine triphosphatase (ATPase), Ca 2+ -Mg 2+ -ATPase, membrane potential (ΔΨm), and membrane fluidity of the liver mitochondrial were estimated. Results: SMO decreased levels of TRIG and CHOL in aging mice. SMO administration elevated the activities of SOD, GSH-Px, and T-AOC, which are suppressed by aging. The levels of MAO and MDA in the liver and brain were reduced by SMO administration in aging mice. Enzyme linked immunosorbent assay showed that SMO significantly decreased the concentration of caspase-3 and improved the activity of Bcl-2 in the liver and brain of aging mice. Furthermore, SMO significantly attenuated the D-gal induced liver mitochondrial dysfunction by improving the activities of Na + -K + -ATPase, Ca 2+ -Mg 2+ -ATPase, membrane potential (ΔΨm), and membrane fluidity. Conclusion: These results indicate that SMO effectively attenuated oxidative damage and improved apoptosis related factors as well as liver mitochondrial dysfunction in aging mice.


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